Substrate-selective protein ectodomain shedding by ADAM17 and iRhom2 depends on their juxtamembrane and transmembrane domains.
ADAM17 (a disintegrin and metalloprotease 17)
EGFR (epidermal growth factor receptor)
Rhbdf1/2 (rhomboid family member 1/2)
TGFα (transforming growth factor α)
TNFα (tumor necrosis factor α)
iRhom1/2 (inactive Rhomboid like protein 1/2)
Journal
FASEB journal : official publication of the Federation of American Societies for Experimental Biology
ISSN: 1530-6860
Titre abrégé: FASEB J
Pays: United States
ID NLM: 8804484
Informations de publication
Date de publication:
04 2020
04 2020
Historique:
received:
18
10
2019
revised:
09
01
2020
accepted:
20
01
2020
pubmed:
28
2
2020
medline:
20
1
2021
entrez:
28
2
2020
Statut:
ppublish
Résumé
The metalloprotease ADAM17 (a disintegrin and metalloprotease 17) regulates EGF-receptor and TNFα signaling, thereby not only protecting the skin and intestinal barrier, but also contributing to autoimmunity. ADAM17 can be rapidly activated by many stimuli through its transmembrane domain (TMD), with the seven membrane-spanning inactive Rhomboids (iRhom) 1 and 2 implicated as candidate regulatory partners. However, several alternative models of ADAM17 regulation exist that do not involve the iRhoms, such as regulation through disulfide bond exchange or through interaction with charged phospholipids. Here, we report that a non-activatable mutant of ADAM17 with the TMD of betacellulin (BTC) can be rescued by restoring residues from the ADAM17 TMD, but only in Adam17
Identifiants
pubmed: 32103528
doi: 10.1096/fj.201902649R
pmc: PMC7316530
mid: NIHMS1552755
doi:
Substances chimiques
Carrier Proteins
0
iRhom2 protein, mouse
0
ADAM17 Protein
EC 3.4.24.86
Adam17 protein, mouse
EC 3.4.24.86
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
4956-4969Subventions
Organisme : NIGMS NIH HHS
ID : R01 GM064750
Pays : United States
Organisme : NIGMS NIH HHS
ID : R35 GM134907
Pays : United States
Informations de copyright
© 2020 Federation of American Societies for Experimental Biology.
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